Micronutrients Part 1A Flashcards

1
Q

what defines group 1 micronutrients?

A

bind to and control type 2 steroid hormone receptors

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2
Q

what are examples of group 1 micronutrients? and which ones DIRECTLY interact with type II receptors?

A

vitamin A, calcium, vitamin D, selenium, iodine, fluoride, phosphorous, vitamin K (only bioactive forms of vit A, vit D and iodine)

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3
Q

In summary, what is the purpose of iodine?

A

Makes T3, which regulates synthesis of proteins that control thyroid function and BMR

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4
Q

In summary, what is the purpose of vit A (hint: 3) ?

A

regulate night vision, epithelial differentiation, gene expression

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5
Q

In summary, what is the purpose of vitamin D?

A

converted to calcitriol, regulates calcium levels in the body

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6
Q

What are type II steroid hormone receptors?

A

found in the nucleus. respond to ligands such as thyroid hormone, retinoic acid, and calcitriol

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7
Q

how much iodine is in each gram of potassium iodide fortified salt?

A

0.03g iodine per g salt

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8
Q

Where is the most iodine in our body found and how much ~?

A

thyroid gland (70-80%)

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9
Q

iodide is immediately converted to its ionic form, I-. The uptake of I- into the blank is mediated by an blank system that uses blank symporter.

A

thyroid gland, active transport, Na+/I- (NIS)

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10
Q

iodine contributes to the production of both T3 and T4. The T4 produced is converted to T3 by 5’deiodinase. The micronutrient blank is required for this conversion.

A

selenium

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11
Q

a patient is suffering from hypothyroidism. which hormone will be tested in their blood?

A

T4. T4 is more abundant than T3 and has a longer half-life

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12
Q

A patient has low T3 and T4, however is getting enough iodine and selenium. What could be the issue?

A

there could be some problem with the hypothalamus/ pituitary gland to signal the production TSH, or an issue with the thyroid recognizing TSH

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13
Q

what hormone interacts with T3 to regulate metabolic rate and growth of tissues?

A

thyroid hormone receptor (THR)

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14
Q

Where is T4 converted to T3?

A

liver

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15
Q

once in the thyroid, what amino acid of which protein interacts with iodine? how? what is the product? where does it occur specifically?

A

tyrosine of the thyroglobulin (THG) protein, iodide radical interacts with the ring of tyrosine to form cross-linking tyrosine residues, products are T4 and T3, occurs specifically in the colloid of the thyroid

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16
Q

Which hormone promotes the following processes:
- lipolysis
- bone production
- increase in heart rate
- muscle contraction
- nutrient digestion

17
Q

Hypothyroidism is the over-production of blank in the thyroid caused by a significant deficiency in blank.

A

TSH, iodine

18
Q

When a fetus in the womb is deficient in iodine, this can cause which disease? What are the symptoms?

A

Cretinism
- growth abnormalities
- intellectual disabilities

19
Q

What are the major forms of Vit A in the body? (4)

A

Retinol, Retinal, Retinyl ester, Retinoic acid

20
Q

What are carotenes? What is their role in human nutrition?

A
  • Carotenes are precursors of vit A (provitamins)
  • ex. beta-carotene
  • founds in plants –> convert to bioactive form of vit A when consumed by animals
21
Q

What is the function and composition of retinyl esters? How does it enter the intestinal mucosal cell (enterocyte)? What enzyme is involved? How is it packaged in the intestinal cell?

A
  • REs are a safe form of vit A (stable)
  • main purpose is storage (have no direct function in the body)
  • RE = retinol + fatty acid
  • Retinyl esterase cleaves the fatty acid
  • Retinol enters the intestinal enterocyte via passive diffusion (incorporated into micelles)
  • Retinal is converted back into RE
    (if not being used, stored in the hepatic stellate cells, ie. liver cells)
  • RE is then packaged into chylomicrons
22
Q

What are the two fates of B-carotene once it enters the intestinal enterocyte? What is this dependent on?

A
    • converted into retinal via the 15-15’-DO enzyme
    • converted into retinol
    • directly packaged into chylomicrons and sent to the liver
    • packaged in VLDL then stored in adipose tissue
    • cause hypercarotenosis (orange skin)

–> Depends on Vit A status of the person
- if deficient, B-carotene will be converted to vit A

23
Q

What is the fate of RE once packaged into chylomicrons?

A
  • transported to the liver
  • converted to retinol (via retinyl esterase)
  • retinol + retinol-binding protein (RBP) = retinol-RBP
24
Q

What is the function of RBP? What does its synthesis depend on?

A
  • RBP is used to transport retinol (Vit A) through the blood to the target tissue.
  • RBP synthesis depends on person’s Vit A status
25
Q

Describe the possible pathways B-carotene once converted into all-trans retinal via 15,15’-DO enzyme?

A
    • converted into all-trans retinol via retinol dehydrogenase
    • esterified into RE
    • follows the pathways of RE
  1. -converted into all-trans retinoic acid
26
Q

What is the sole purpose of retinal? how does this occur? where does this occur?

A

-all trans retinol is converted to 11-cis retinal (in the eye)
- 11-cis retinal is converted to Rhodopsin
- When exposed to light,
Rhodopsin –> Opsin + all-trans retinal
- This phenomenon sends neural signals that induce VISION!
- Both opsin and all trans retinal are recycled in the Interphotoreceptor matrix

27
Q

What are photoreceptor (Rod) cells and how do they absorb to light?

A

Photoreceptor (Rod) cells in the retina detect and convert light into neural signals that induce vision. They use Rhodopsin to absorb light.

28
Q

What is the function of Retinoic acid?

A
  • RA binds to and activates RAR (retinoic acid receptor)
  • stimulated growth hormones
  • creates a large combination of transcription factors
  • good regulation of gene expression and differentiation of cells
29
Q

What is a symptom of Vit A deficiency at the cellular level?

A
  • poor cell differentiation
  • keratinization, but no mucus secretion
  • no mucus causes a weak epithelial layer that is susceptible to bacteria and viruses
30
Q

What is keratin? What is keratinization? What are the causes and symptoms?

A
  • A major protein expressed in the epithelial cells
  • build of keratin in the epithelial cells that makes them tough and water-resistant
  • lack of mucous
  • caused by vit A deficiency (specifically RA deficiency)
31
Q

What is the most severe consequence of vit A toxicity? What drug is known to cause vit A toxicity in pregnant women?

A
  • liver cell death
  • Vit A spills out and damages nearby liver cells
  • Accutane has too much vit A (13-cis retinoic acid), known to cause birth defects in pregnant women